TGI Friday! Our weekly round-up of recently published research abstracts | 21 October 2016

October 21, 2016


From the Journal of Nature and Science (open access), October 2016.

Elevated Energy Production in Chronic Fatigue Syndrome Patients.

Nick Lawson(1), Chung-Han Hsieh(1), Dana March(2), Xinnan Wang(1*).
1) Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA.
2) Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.
* Corresponding Author. Email: xinnanw@stanford.edu

Abstract

Chronic Fatigue Syndrome (CFS) is a debilitating disease characterized by physical and mental exhaustion. The underlying pathogenesis is unknown, but impairments in certain mitochondrial functions have been found in some CFS patients.

To thoroughly reveal mitochondrial deficiencies in CFS patients, here we examine the key aspects of mitochondrial function in blood cells from a paired CFS patient-control series.

Surprisingly, we discover that in patients the ATP levels are higher and mitochondrial cristae are more condensed compared to their paired controls, while the mitochondrial crista length, mitochondrial size, shape, density, membrane potential, and enzymatic activities of the complexes in the electron transport chain remain intact.

We further show that the increased ATP largely comes from non-mitochondrial sources.

Our results indicate that the fatigue symptom in this cohort of patients is unlikely caused by lack of ATP and severe mitochondrial malfunction. On the contrary, it might be linked to a pathological mechanism by which more ATP is produced by non-mitochondrial sources.


1 thought on “TGI Friday! Our weekly round-up of recently published research abstracts | 21 October 2016”

  1. This is seriously poor science!! On a potentially dysfunctioning system displaying reactive hypertrophy they pour a super-soup of vitamins, minerals and co-factors (DMEM) and then measure ‘increased’ energy production. They then make that ‘increased energy production’ their title of their paper without considering the possibility that the hypertrophy and increased density of the mitochondria and their cristae is a response to poorly functioning energy pathways and enzymes within and around the mitochondria that may (many think probably) be deficient in said vitamins, minerals and co-factors! The measured increase in energy production in the experiment is thus a reflection of the lack of energy production in vivo due to magnesium, zinc, manganese, B1, B2, B5, B6, B9, PQQ, Fe, ….(and so on) deficiency?

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